Pathogenesis of insulin resistance in skeletal muscle.

Pathogenesis of insulin resistance in skeletal muscle.
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DOI:
10.1155/2010/476279
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发表时间:
2010
影响因子:
--
通讯作者:
DeFronzo RA
DeFronzo RA
中科院分区:
其他
文献类型:
--
作者:
Abdul-Ghani MA;DeFronzo RA

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骨骼肌中的胰岛素抵抗表现为胰岛素刺激的葡萄糖摄取减少,并且是由受损的胰岛素信号传导和多种受体后细胞内缺陷(包括受损的葡萄糖转运、葡萄糖磷酸化和减少的葡萄糖氧化和糖原合成)引起的。胰岛素抵抗是2型糖尿病的核心缺陷,也与肥胖和代谢综合征有关。脂肪酸代谢失调在骨骼肌胰岛素抵抗的发病机制中起着关键作用。最近的研究报道了各种胰岛素抵抗状态下骨骼肌中线粒体氧化磷酸化缺陷。本文综述了导致骨骼肌胰岛素抵抗的细胞和分子缺陷。
Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Insulin resistance is a core defect in type 2 diabetes, it is also associated with obesity and the metabolic syndrome. Dysregulation of fatty acid metabolism plays a pivotal role in the pathogenesis of insulin resistance in skeletal muscle. Recent studies have reported a mitochondrial defect in oxidative phosphorylation in skeletal muscle in variety of insulin resistant states. In this review, we summarize the cellular and molecular defects that contribute to the development of insulin resistance in skeletal muscle.
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